But how does AB really work?

Im really stoked about Anabeta being released since I so far has loved all your products. But even though the info is here I find it a bit unclear how it works. Since its anabolic and not in a steroidal way, is it a SARM? Is it possible to get more specific detailes on the way of action?

Its effects would be considered non-AR mediated anabolic. Even in anabolics that have been researched for years and in humans that have significant non-AR mediated effects the exact non-AR effects are yet to be determined. But Bill Roberts suspects "Unfortunately we cannot yet identify how many non-AR-mediated activities there may be. There are I think at least two: activity in microsomes and activities in nerves. There may be more. For example, differentiation of satellite cells of muscle into mature muscle cells might be a non-AR mediated activity."

This is a quote in reference to non-AR mediated steroids, not AnaBeta.

Its effects would be considered non-AR mediated anabolic. Even in anabolics that have been researched for years and in humans that have significant non-AR mediated effects the exact non-AR effects are yet to be determined. But Bill Roberts suspects "Unfortunately we cannot yet identify how many non-AR-mediated activities there may be. There are I think at least two: activity in microsomes and activities in nerves. There may be more. For example, differentiation of satellite cells of muscle into mature muscle cells might be a non-AR mediated activity."

This is a quote in reference to non-AR mediated steroids, not AnaBeta.

Precisely.

Ive never noticed too much from ecdy unfortunately, so I'm not sure if there would be too much synergy there.

Ecdy has never really produced real world results IMO...could be synergistic but also I would not want to risk any competition in the body between the two.

I would just use AnaBeta by itself. Some BCAAs or LCLT if you want to stack it with something

Have you ever tried E-BOL? There are so many logs out there now, it used to be hard to find quality information on its effects. I have personally used E-BOL and had great success. To each their own though, not all supps work the same way with everybody. You have to know your natural response.

The biological activity of testosterone and dihydrotestosterone is thought to occur predominantly through binding to the androgen receptor (AR), a
member of the nuclear receptor superfamily that functions as a ligand-activated transcription factor. However, androgens have also been reported
to induce the rapid activation of kinase-signaling cascades and modulate intracellular calcium levels. These effects are considered to be nongenomic because they occur in cell types that lack a functional AR, in the presence of inhibitors of transcription and translation, or are observed to
occur too rapidly to involve changes in gene transcription. Such nongenomic effects of androgens may occur through AR functioning in the cytoplasm to induce the MAPK signal cascade. In addition, androgens may function through the sex hormone binding globulin receptor and possibly a
distinct G protein-coupled receptor to activate second messenger signaling mechanisms. The physiological effect of nongenomic androgen action has yet to be determined. However, it may ultimately contribute to regulation of transcription factor activity, including mediation of the transcriptional activity of AR. (Molecular Endocrinology 16: 2181–2187, 2002).

I dont expect anyone to fully understand that, but rather just trust what we are trying to explain

The biological activity of testosterone and dihydrotestosterone is thought to occur predominantly through binding to the androgen receptor (AR), a
member of the nuclear receptor superfamily that functions as a ligand-activated transcription factor. However, androgens have also been reported
to induce the rapid activation of kinase-signaling cascades and modulate intracellular calcium levels. These effects are considered to be nongenomic because they occur in cell types that lack a functional AR, in the presence of inhibitors of transcription and translation, or are observed to
occur too rapidly to involve changes in gene transcription. Such nongenomic effects of androgens may occur through AR functioning in the cytoplasm to induce the MAPK signal cascade. In addition, androgens may function through the sex hormone binding globulin receptor and possibly a
distinct G protein-coupled receptor to activate second messenger signaling mechanisms. The physiological effect of nongenomic androgen action has yet to be determined. However, it may ultimately contribute to regulation of transcription factor activity, including mediation of the transcriptional activity of AR. (Molecular Endocrinology 16: 2181–2187, 2002).

I dont expect anyone to fully understand that, but rather just trust what we are trying to explain

Cliffs: There are secondary non-AR binding pathways that lead to growth.

If youre referring strictly to androgens, there are several with low AR affinity that still produce HPTA suppression. There are, however, many secondary pathways for producing anabolism without affecting the AR (Igf-1, myostatin inhibitors, beta2 agonists, etc.) The non-AR specific pathways are very complex, and some androgens could still be precursors to ones with high AR affinity, but we feel the mechanisms behind AnaBeta lie in the non-AR mediated route.

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If youre referring strictly to androgens, there are several with low AR affinity that still produce HPTA suppression. There are, however, many secondary pathways for producing anabolism without affecting the AR (Igf-1, myostatin inhibitors, beta2 agonists, etc.) The non-AR specific pathways are very complex, and some androgens could still be precursors to ones with high AR affinity, but we feel the mechanisms behind AnaBeta lie in the non-AR mediated route.

Thanks for the clarification, that's what I was trying to get at. AnaBeta basically produces anabolic effects but not necessarily through direct binding to the AR, so it won't compete with and suppress testosterone.

Originally Posted by nattydisaster

Correct. This would A) avoid competition with testosterone on the AR and B) keep from any negative feedback inhibition on HPTA

Cool, got it.

Now the $1M question is which secondary pathway is being used (IGF-1, GH, MGF, myostatin, others)? That's a tough one, and ultimately not that important IMO (some better than others) as long as the results work out with no real negative sides.

But those androgenic sides cited in the study were likely due to increased testosterone levels, right? Hard to say for sure, but it seemed like it could've been a factor.

Unlikely. If you look at the 100 group when their bw and testes weight are over that of athe group taking testosterone the prostate weight is significantly lower. If it were just an increase in testosterone the prostate weight would be greater than the testosterone group. Compare the 50 group as well to the testosterone group and you'll see the same thing